The purpose of this study was to reveal synaptic plasticity within the dorsal cochlear nucleus (DCN) as
a result of noise trauma and to determine whether effective antioxidant protection to the cochlea can
also impact plasticity changes in the DCN. Expression of synapse activity markers (synaptophysin and
precerebellin) and ultrastructure of synapses were examined in the DCN of chinchilla 10 days after
a 105 dB SPL octave-band noise (centered at 4 kHz, 6 h) exposure. One group of chinchilla was treated
with a combination of antioxidants (4-hydroxy phenyl N-tert-butylnitrone, N-acetyl-L-cysteine and
acetyl-L-carnitine) beginning 4 h after noise exposure. Down-regulated synaptophysin and precerebellin
expression, as well as selective degeneration of nerve terminals surrounding cartwheel cells and their
primary dendrites were found in the fusiform soma layer in the middle region of the DCN of the noise
exposure group. Antioxidant treatment significantly reduced synaptic plasticity changes surrounding
cartwheel cells. Results of this study provide further evidence of acoustic trauma-induced neural plasticity
in the DCN and suggest that loss of input to cartwheel cells may be an important factor contributing
to the emergence of hyperactivity in the DCN after noise exposure. Results further suggest that early
antioxidant treatment for acoustic trauma not only rescues cochlear hair cells, but also has impact on
central auditory structures.